As is widely appreciated throughout the pharmaceutical industry, the risk of acquired torsade de pointes arrhythmia (TdP) is proportional to the fractional decrease in the outward repolarizing current (denoted IKr) of the human ether-a-go-go gene product K+ channel (hERG) [1–5] due to occupancy of the ion conduction pathway by hERG-blocking drugs. Here, KCNH2 is linked to torsades de pointes.